Natriuretic and diuretic action of centrally administered rat atrial natriuretic peptide (99–126): possible involvement of aldosterone and the sympathoadrenal system

Abstract

Intracerebroventricular (ICV) administration of rat atrial natriuretic peptide (99-126) (rANP) to conscious male hydrated rats resulted in a dose-related increase in urinary volume and sodium excretion over a 6-h period of urine collection. A diminished mineralocorticoid effect on the kidneys may explain the natriuretic phenomenon. This hypothesis was tested by ICV rANP injection (1.25 microgram/5 microL) in conscious hydrated rats pretreated beforehand with d-aldosterone (20 micrograms/kg, ip). Although the absolute amount of sodium excreted was reduced, aldosterone did not affect rANP-induced sodium output at 1 and 3 h. Rats that were sham-operated or bilaterally adrenalectomized after 4 days were pretreated with aldosterone and given an oral water load followed by ICV rANP or saline. The possible participation of the peripheral sympathetic nervous system in the central action of rANP was evaluated in rats pretreated with 6-hydroxydopamine. In sympathectomized and adrenalectomized rats natriuresis and diuresis were still evident after rANP. Our results indicate that the natriuretic effect of ICV rANP is independent of mineralocorticoids. Likewise, diuresis and natriuresis can occur in the absence of the adrenal glands and are independent from the neural tone that the adrenergic system exerts on sodium reabsorption.

Effect of Water and Saline Load on Urinary Output in Healthy Undergraduate Medical Students

“…3 Diuresis and natriuresis are known to occur in the absence of the adrenal glands and are independent from the neural tone that the adrenergic system exerts on sodium reabsorption. 4 The diuretic response in the present study therefore might have occurred due to increase in blood volume leading to pressure diuresis. The release of atrial natriuretic peptide might have contributed to diuresis minimally since there was no significant change in specific gravity.…”

Atrial natriuretic peptide (ANP) as a neuropeptide: interaction with angiotensin II on volume control and renal sodium handling.

“…Central infusion of ANP has been reported to have no effect on Na+ excretion whilst a single ventricular dose of ANP was reported to elicit an increase in Na+ excretion independent of mineralocorticoid and neural function (Israel et al, 1988). Similarly, natriuresis was also reported to occur in response to centrally administered ANP in conscious sheep (Parks et al, 1988).…”

Atrial natriuretic peptide in the subfornical organ reduces drinking induced by angiotensin or in response to water deprivation.

“…Injections or infusions of ANP into the forebrain ventricles reduce drinking induced by angiotensin or in response to water deprivation (Antunes-Rodrigues, McCann, Rogers, & Samson, 1985; Katsuura et al, 1986; Masotto & Negro-Vilar, 1985; Nakamura, Katsuura, Nakao, & Imura, 1985) and reduce salt appetite induced by angiotensin or in response to sodium depletion (Antunes-Rodriguess, McCann, & Samson, 1986; Fitts, Thunhorst, & Simpson, 1985; Itoh et al, 1986; Masotto & Negro-Vilar, 1985). Intraventricular ANP is mildly diuretic in rats at doses that are not diuretic peripherally (Fitts et al, 1985; Israel & Barbella, 1986; Israel, Torres, & Barbella, 1988; Lee, Feng, Malvin, Huang, & Grekin, 1987). Secretion of several endocrines, such as vasopressin, oxytocin, prolactin, and luteinizing hormone, is affected by central ANP injections (Casto, Keiler, Schroeder, & Stock, 1987; Poole, Carter, Vallejo, & Lightman, 1987; Samson, Aguila, Martinovic, Antunes-Rodrigues, & Norris, 1987; Samson & Bianchi, 1988; Steele, 1988).…”